In studying this possible pathway of seizures, Alexander made an important finding about its organization. It was already known that cells in the thalamus communicate with cells in the cortex by releasing the neurotransmitter glutamate. The glutamate travels across the gap -- creating a pathway for cell-to-cell communication.
Alexander and Godwin were the first to show that in addition to releasing glutamate, thalamus cells also have a special type of glutamate receptor that acts almost as a braking system slowing the release of glutamate when there is high-intensity brain activity associated with a seizure.
"It's like the gas and brake pedals of your car, "said Godwin, associate professor of neurobiology and anatomy and the senior researcher on the project. "Glutamate is important for normal communication in the brain, but sometimes it's necessary to put on the brakes in order to preserve normal function. This receptor appears to slow down the rate at which glutamate is released across the synaptic gap, and may protect the cells from becoming overexcited."
Alexander hypothesizes that in epilepsy patients, the protective receptors may not function well or that glutamate production may be abnormal. A treatment that targets these protective glutamate receptors has the potential to block the pathway involved in seizures, with the added benefit of allowing normal communication to continue.
"If this research leads to drugs that can target these newly discovered receptors, it would be an important advance in therapy," said William L. Bell, M.D., a specialist in epilepsy at Wake Forest University Baptist Medical Center.
Godwin explained that design of improved drugs to target the receptors wouldn't be a cure, but would short-circuit the type of abnormal activity that results in seizures.
In this research
'"/>
Contact: Shannon Koontz
shkoontz@wfubmc.edu
336-716-2415
Wake Forest University Baptist Medical Center
1-Jul-2005